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A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Public Health Microbiology".

Deadline for manuscript submissions: 15 March 2025 | Viewed by 16366

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Dr. Célio Geraldo Freire-de-Lima

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Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-902, Brazil
Interests: glycobiology of fungi
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Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to this Special Issue entitled “Parasitic Infection and Host Immunity 2.0”. Infectious diseases are diseases caused by microorganisms such as viruses, bacteria, protozoa, or fungi, which can be present in the body without causing any damage to the body. However, when there is some change in the host immune system and other clinical conditions, these microorganisms can proliferate, causing disease and facilitating the entry of other microorganisms.

Infectious and contagious diseases can be caused by viruses, fungi, bacteria, or parasites and, depending on the infectious agent, can cause diseases with specific symptoms. Among the main infectious diseases, the following can be mentioned:

1) Infectious diseases caused by viruses; 2) Infectious diseases caused by bacteria; 3) Infectious diseases caused by fungi; 4) Infectious diseases caused by protozoa; 5) Infectious diseases caused by helminths.

Depending on the microorganism causing the disease, characteristic signs and symptoms of the disease may appear, the most common being headache, fever, nausea, weakness, and feeling unwell and tired, especially in the initial phase of the infectious process. However, depending on the disease, more serious symptoms may appear, such as an enlarged liver, stiff neck, convulsions, and coma, for example. Infectious diseases can be acquired through direct contact with the infectious agent or through exposure of the person to contaminated water or food as well as through respiratory, sexual, or animal injuries. These diseases can also often be transmitted from person to person, and are termed infectious diseases in these cases.

This Special Issue aims to review or describe the latest findings regarding the immunopathology, epidemiology, and diagnostic tools in parasitic infection of microorganisms and host immunity. The ultimate goal is to provide readers with new insights into the current and future state of the diagnosis and treatment procedures and pathologies for these diseases.

For this Special Issue, original research articles and reviews are welcome. Research areas of interest may include (but are not limited to) the following: epidemiology of human and animal infectious diseases, immunopathology of human and animal infectious diseases, and clinical treatment and diagnosis of humans. We look forward to receiving your contributions.

Dr. Célio Geraldo Freire-de-Lima
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Microorganisms is an international peer-reviewed open access monthly journal published by MDPI.

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Keywords

infectious diseases
parasite infection
host-parasite interaction
immunomodulation
immunopathology
epidemiology

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Published Papers (7 papers)

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19 pages, 2890 KiB

Open AccessArticle

A Comparative Analysis of Innate Immune Responses and the Structural Characterization of Spike from SARS-CoV-2 Gamma Variants and Subvariants

by Aline Miranda Scovino, Elizabeth Chen Dahab, Israel Diniz-Lima, Etiele de Senna Silveira, Shana Priscila Coutinho Barroso, Karina Martins Cardoso, Dirlei Nico, Gustavo José Makhoul, Elias Barbosa da Silva-Junior, Celio Geraldo Freire-de-Lima, Leonardo Freire-de-Lima, Leonardo Marques da Fonseca, Natalia Valente, Valeria Nacife, Ana Machado, Mia Araújo, Gustavo Fioravanti Vieira, Alex Pauvolid-Corrêa, Marilda Siqueira and Alexandre Morrot

Microorganisms 2024, 12(4), 720; https://doi.org/10.3390/microorganisms12040720 - 2 Apr 2024

Viewed by 1909

Abstract

The SARS-CoV-2 P.1 variant, responsible for an outbreak in Manaus, Brazil, is distinguished by 12 amino acid differences in the S protein, potentially increasing its ACE-2 affinity and immune evasion capability. We investigated the innate immune response of this variant compared to the original B.1 strain, particularly concerning cytokine production. Blood samples from three severe COVID-19 patients were analyzed post-infection with both strains. Results showed no significant difference in cytokine production of mononuclear cells and neutrophils for either variant. While B.1 had higher cytopathogenicity, neither showed viral replication in mononuclear cells. Structural analyses of the S protein highlighted physicochemical variations, which might be linked to the differences in infectivity between the strains. Our studies point to the increased infectivity of P.1 could stem from altered immunogenicity and receptor-binding affinity. Full article

(This article belongs to the Special Issue Parasitic Infection and Host Immunity, 2nd Edition)

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14 pages, 3444 KiB

Open AccessArticle

Transcriptome Analysis Identifies the Crosstalk between Dendritic and Natural Killer Cells in Human Cutaneous Leishmaniasis

by Sara Nunes, Rafael Tibúrcio, Icaro Bonyek-Silva, Pablo Rafael Oliveira, Ricardo Khouri, Viviane Boaventura, Aldina Barral, Cláudia Brodskyn and Natalia Machado Tavares

Microorganisms 2023, 11(8), 1937; https://doi.org/10.3390/microorganisms11081937 - 29 Jul 2023

Cited by 1 | Viewed by 1579

Abstract

Skin ulcers of cutaneous leishmaniasis (CL) are characterized by a localized inflammatory response mediated by innate and adaptive immune cells, including dendritic cells (DC) and natural killer (NK) cells. Bidirectional interactions between DCs and NK cells contribute to tailor leishmaniasis outcome. Despite advances in the Leishmania biology field in recent decades, the mechanisms involved in DC/NK-mediated control of Leishmania sp. pathogenesis as well as the cellular and molecular players involved in such interaction remain unclear. The present study sought to investigate canonical pathways associated with CL arising from Leishmania braziliensis infection. Initially, two publicly available microarray datasets of skin biopsies from active CL lesions were analyzed, and five pathways were identified using differentially expressed genes. The “Crosstalk between DCs and NK cells” pathway was notable due to a high number of modulated genes. The molecules significantly involved in this pathway were identified, and our findings were validated in newly obtained CL biopsies. We found increased expression of TLR4, TNFRSF1B, IL-15, IL-6, CD40, CCR7, TNF and IFNG, confirming the analysis of publicly available datasets. These findings reveal the “crosstalk between DCs and NK cells” as a potential pathway to be further explored in the pathogenesis of CL, especially the expression of CCR7, which is correlated with lesion development. Full article

(This article belongs to the Special Issue Parasitic Infection and Host Immunity, 2nd Edition)

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21 pages, 5670 KiB

Open AccessArticle

Cytokine Responses during Mycobacterium tuberculosis H37Rv and Ascaris lumbricoides Costimulation Using Human THP-1 and Jurkat Cells, and a Pilot Human Tuberculosis and Helminth Coinfection Study

by Khethiwe N. Bhengu, Ravesh Singh, Pragalathan Naidoo, Miranda N. Mpaka-Mbatha, Nomzamo Nembe-Mafa and Zilungile L. Mkhize-Kwitshana

Microorganisms 2023, 11(7), 1846; https://doi.org/10.3390/microorganisms11071846 - 21 Jul 2023

Cited by 4 | Viewed by 2136

Abstract

Background: Helminth infections are widespread in tuberculosis-endemic areas and are associated with an increased risk of active tuberculosis. In contrast to the pro-inflammatory Th1 responses elicited by Mycobacterium tuberculosis (Mtb) infection, helminth infections induce anti-inflammatory Th2/Treg responses. A robust Th2 response has been linked to reduced tuberculosis protection. Several studies show the effect of helminth infection on BCG vaccination and TB, but the mechanisms remain unclear. Aim: To determine the cytokine response profiles during tuberculosis and intestinal helminth coinfection. Methods: For the in vitro study, lymphocytic Jurkat and monocytic THP-1 cell lines were stimulated with Mtb H37Rv and Ascaris lumbricoides (A. lumbricoides) excretory-secretory protein extracts for 24 and 48 h. The pilot human ex vivo study consisted of participants infected with Mtb, helminths, or coinfected with both Mtb and helminths. Thereafter, the gene transcription levels of IFN-γ, TNF-α, granzyme B, perforin, IL-2, IL-17, NFATC2, Eomesodermin, IL-4, IL-5, IL-10, TGF-β and FoxP3 in the unstimulated/uninfected controls, singly stimulated/infected and costimulated/coinfected groups were determined using RT-qPCR. Results: TB-stimulated Jurkat cells had significantly higher levels of IFN-γ, TNF-α, granzyme B, and perforin compared to unstimulated controls, LPS- and A. lumbricoides-stimulated cells, and A. lumbricoides plus TB-costimulated cells (p < 0.0001). IL-2, IL-17, Eomes, and NFATC2 levels were also higher in TB-stimulated Jurkat cells (p < 0.0001). Jurkat and THP-1 cells singly stimulated with TB had lower IL-5 and IL-4 levels compared to those singly stimulated with A. lumbricoides and those costimulated with TB plus A. lumbricoides (p < 0.0001). A. lumbricoides-singly stimulated cells had higher IL-4 levels compared to TB plus A. lumbricoides-costimulated Jurkat and THP-1 cells (p < 0.0001). TGF-β levels were also lower in TB-singly stimulated cells compared to TB plus A. lumbricoides-costimulated cells (p < 0.0001). IL-10 levels were lower in TB-stimulated Jurkat and THP-1 cells compared to TB plus A. lumbricoides-costimulated cells (p < 0.0001). Similar results were noted for the human ex vivo study, albeit with a smaller sample size. Conclusions: Data suggest that helminths induce a predominant Th2/Treg response which may downregulate critical Th1 responses that are crucial for tuberculosis protection. Full article

(This article belongs to the Special Issue Parasitic Infection and Host Immunity, 2nd Edition)

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21 pages, 3140 KiB

Open AccessArticle

Is There Any Difference in the In Situ Immune Response in Active Localized Cutaneous Leishmaniasis That Respond Well or Poorly to Meglumine Antimoniate Treatment or Spontaneously Heal?

by Jéssica Leite-Silva, Carla Oliveira-Ribeiro, Fernanda Nazaré Morgado, Maria Inês Fernandes Pimentel, Marcelo Rosandiski Lyra, Aline Fagundes, Luciana Freitas Campos Miranda, Claudia Maria Valete-Rosalino, Armando Oliveira Schubach and Fátima Conceição-Silva

Microorganisms 2023, 11(7), 1631; https://doi.org/10.3390/microorganisms11071631 - 22 Jun 2023

Cited by 1 | Viewed by 1345

Abstract

Localized cutaneous leishmaniasis caused by Leishmania braziliensis can either respond well or poorly to the treatment or heal spontaneously; It seems to be dependent on the parasite and/or host factors, but the mechanisms are not fully understood. We evaluated the in situ immune response in eighty-two active lesions from fifty-eight patients prior to treatment classified as early spontaneous regression (SRL-n = 14); treatment responders (GRL-n = 20); and non-responders (before first treatment/relapse, PRL1/PRL2-n = 24 each). Immunohistochemistry was used to identify cell/functional markers which were correlated with the clinical characteristics. PRL showed significant differences in lesion number/size, clinical evolution, and positive parasitological examinations when compared with the other groups. SRL presented a more efficient immune response than GRL and PRL, with higher IFN-γ/NOS2 and a lower percentage of macrophages, neutrophils, NK, B cells, and Ki-67+ cells. Compared to SRL, PRL had fewer CD4+ Tcells and more CD163+ macrophages. PRL1 had more CD68+ macrophages and Ki-67+ cells but less IFN-γ than GRL. PRL present a less efficient immune profile, which could explain the poor treatment response, while SRL had a more balanced immune response profile for lesion healing. Altogether, these evaluations suggest a differentiated profile of the organization of the inflammatory process for lesions of different tegumentary leishmaniasis evolution. Full article

(This article belongs to the Special Issue Parasitic Infection and Host Immunity, 2nd Edition)

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14 pages, 3074 KiB

Open AccessArticle

Gene Signatures of Symptomatic and Asymptomatic Clinical-Immunological Profiles of Human Infection by Leishmania (L.) chagasi in Amazonian Brazil

by Vania Lucia R. da Matta, André N. Gonçalves, Cláudia Maria C. Gomes, Islam H. Chouman, Frederico M. Ferreira, Marliane B. Campos, Luciana V. Lima, Thiago Vasconcelos dos Santos, Patrícia Karla Ramos, Rodrigo R. Furtado, Marcia D. Laurenti, Carlos Eduardo P. Corbett, Helder I. Nakaya and Fernando T. Silveira

Microorganisms 2023, 11(3), 653; https://doi.org/10.3390/microorganisms11030653 - 3 Mar 2023

Cited by 1 | Viewed by 2127

Abstract

Individuals infected with Leishmania (L.) chagasi may present different asymptomatic and symptomatic stages of infection, which vary in the clinical–immunological profiles that can be classified as asymptomatic infection (AI), subclinical resistant infection (SRI), indeterminate initial infection (III), subclinical oligosymptomatic infection (SOI), and symptomatic infection (SI) (=American visceral leishmaniasis, AVL). However, little is known about the molecular differences between individuals having each profile. Here, we performed whole-blood transcriptomic analyses of 56 infected individuals from Pará State (Brazilian Amazon), covering all five profiles. We then identified the gene signatures of each profile by comparing their transcriptome with those of 11 healthy individuals from the same area. Symptomatic individuals with SI (=AVL) and SOI profiles showed higher transcriptome perturbation when compared to those asymptomatic III, AI and SRI profiles, suggesting that disease severity may be associated with greater transcriptomic changes. Although the expression of many genes was altered on each profile, very few genes were shared among the profiles. This indicated that each profile has a unique gene signature. The innate immune system pathway was strongly activated only in asymptomatic AI and SRI profiles, suggesting the control of infection. In turn, pathways such as MHC Class II antigen presentation and NF-kB activation in B cells seemed to be specifically induced in symptomatic SI (=AVL) and SOI profiles. Moreover, cellular response to starvation was down-regulated in those symptomatic profiles. Overall, this study revealed five distinct transcriptional patterns associated to the clinical–immunological (symptomatic and asymptomatic) profiles of human L. (L.) chagasi-infection in the Brazilian Amazon. Full article

(This article belongs to the Special Issue Parasitic Infection and Host Immunity, 2nd Edition)

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9 pages, 273 KiB

Open AccessCase Report

Trypanosoma cruzi DNA Identification in Breast Milk from Mexican Women with Chagas Disease

by María del Pilar Crisóstomo-Vázquez, Griselda Rodríguez-Martínez, Verónica Jiménez-Rojas, Leticia Eligio-García, Alfonso Reyes-López, María Hernández-Ramírez, Francisco Hernández-Juárez, José Luis Romero-Zamora, Silvia Guadalupe Vivanco-Tellez, Fortino Solorzano-Santos, Victor M. Luna-Pineda and Guillermina Campos-Valdez

Microorganisms 2024, 12(12), 2660; https://doi.org/10.3390/microorganisms12122660 - 21 Dec 2024

Viewed by 591

Abstract

(1) Background: Chagas disease is a public health problem affecting nearly 2 million women of reproductive age in Latin America. From these, 4–8% can transmit the infection to the foetus through the vertical route, whereas horizontal transmission through milk during breastfeeding remains controversial. Therefore, the presence of Trypanosoma cruzi (T. cruzi) DNA in the milk of women seropositive for Chagas disease was analysed to determine whether a relationship with the infection of their children can exist. (2) Methods: 260 pairs (mother–child) from four hospitals located in rural areas endemic to T. cruzi (state of Oaxaca) were studied. The presence of anti-T. cruzi antibodies in the serum of lactating women were determined by ELISA, whereas parasitic DNA in either breast milk or newborn’s blood was identified by PCR; (3) Results: The seroprevalence of infection in lactating women was 5.76%, and the frequency of infection detected by PCR in breast milk was 1.92%, while the frequency of infection in the blood of newborns was 1.92%. Pochutla-Oaxaca presented the highest number of positive cases in both breast milk and blood. The only risk factor found was the presence of the vector in the geographical area analysed, favouring the parasite’s transmission. Overall, the results suggest a probable transmission of T. cruzi, although whether it was through breastfeeding or through the blood during delivery could not be determined. (4) Conclusions: T. cruzi DNA was identified in lactating women’s milk and newborn blood, which is probable evidence of transmission through breastfeeding; nevertheless, future studies must be performed to confirm the presence of the parasite, alive or dead. Full article

(This article belongs to the Special Issue Parasitic Infection and Host Immunity, 2nd Edition)

13 pages, 1761 KiB

Open AccessPerspective

Visiting Molecular Mimicry Once More: Pathogenicity, Virulence, and Autoimmunity

by Yuri Chaves Martins, Arnon Dias Jurberg and Cláudio Tadeu Daniel-Ribeiro

Microorganisms 2023, 11(6), 1472; https://doi.org/10.3390/microorganisms11061472 - 1 Jun 2023

Cited by 9 | Viewed by 5401

Abstract

The concept of molecular mimicry describes situations in which antigen sharing between parasites and hosts could benefit pathogen evasion from host immune responses. However, antigen sharing can generate host responses to parasite-derived self-like peptides, triggering autoimmunity. Since its conception, molecular mimicry and the consequent potential cross-reactivity following infections have been repeatedly described in humans, raising increasing interest among immunologists. Here, we reviewed this concept focusing on the challenge of maintaining host immune tolerance to self-components in parasitic diseases. We focused on the studies that used genomics and bioinformatics to estimate the extent of antigen sharing between proteomes of different organisms. In addition, we comparatively analyzed human and murine proteomes for peptide sharing with proteomes of pathogenic and non-pathogenic organisms. We conclude that, although the amount of antigenic sharing between hosts and both pathogenic and non-pathogenic parasites and bacteria is massive, the degree of this antigen sharing is not related to pathogenicity or virulence. In addition, because the development of autoimmunity in response to infections by microorganisms endowed with cross-reacting antigens is rare, we conclude that molecular mimicry by itself is not a sufficient factor to disrupt intact self-tolerance mechanisms. Full article

(This article belongs to the Special Issue Parasitic Infection and Host Immunity, 2nd Edition)

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